中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2010年
9期
1236-1238
,共3页
氯离子电流%新福林%α1-肾上腺素受体激动剂%心房肌细胞
氯離子電流%新福林%α1-腎上腺素受體激動劑%心房肌細胞
록리자전류%신복림%α1-신상선소수체격동제%심방기세포
Chloride current%Phenylephrine%α1-adrenoceptor agonist%Atrial myocyte
目的 通过全细胞膜片钳技术研究α1-肾上腺素受体激动剂新福林对人心房肌细胞肿胀激活的氯离子电流(ICl.swell)的调节作用.方法 术中取冠脉搭桥患者右心耳组织,酶解分离出心房肌细胞.全细胞膜片钳技术记录氯离子电流.等渗、低渗台氏液灌流;分别加入新福林、氯离子电流阻滞剂4,4'-二异硫氰基芪-2,2'-二磺酸(DIDS)、α1受体阻断剂哌唑嗪,观察电流变化.结果 低渗台氏液灌流心房肌细胞,可记录到ICl.swell.用含有100μmol/L新福林的低渗台氏液灌流,ICl.swell电流强度增加.在-90 mV,电流强度由(-1.11±0.55)pA/pF增加到(-1.56±0.69)pA/pF(P＜0.05,n=7);+40mV,由(3.24±2.04)pA/pF增加到(4.64±2.61)pA/pF(P＜0.01,n=7).这种效应为浓度依赖性,加入DIDS或者用等渗灌流液灌流,该效应被逆转.加入哌唑嗪1 μmol/L可以使新福林的量效关系曲线右移.结论 在人心房肌细胞新福林可以增强ICl.swell,这和在其他动物得到的结果不同.该现象是首次发现,表明新福林对ICl.swell的调节具有种属特异性.
目的 通過全細胞膜片鉗技術研究α1-腎上腺素受體激動劑新福林對人心房肌細胞腫脹激活的氯離子電流(ICl.swell)的調節作用.方法 術中取冠脈搭橋患者右心耳組織,酶解分離齣心房肌細胞.全細胞膜片鉗技術記錄氯離子電流.等滲、低滲檯氏液灌流;分彆加入新福林、氯離子電流阻滯劑4,4'-二異硫氰基芪-2,2'-二磺痠(DIDS)、α1受體阻斷劑哌唑嗪,觀察電流變化.結果 低滲檯氏液灌流心房肌細胞,可記錄到ICl.swell.用含有100μmol/L新福林的低滲檯氏液灌流,ICl.swell電流彊度增加.在-90 mV,電流彊度由(-1.11±0.55)pA/pF增加到(-1.56±0.69)pA/pF(P＜0.05,n=7);+40mV,由(3.24±2.04)pA/pF增加到(4.64±2.61)pA/pF(P＜0.01,n=7).這種效應為濃度依賴性,加入DIDS或者用等滲灌流液灌流,該效應被逆轉.加入哌唑嗪1 μmol/L可以使新福林的量效關繫麯線右移.結論 在人心房肌細胞新福林可以增彊ICl.swell,這和在其他動物得到的結果不同.該現象是首次髮現,錶明新福林對ICl.swell的調節具有種屬特異性.
목적 통과전세포막편겸기술연구α1-신상선소수체격동제신복림대인심방기세포종창격활적록리자전류(ICl.swell)적조절작용.방법 술중취관맥탑교환자우심이조직,매해분리출심방기세포.전세포막편겸기술기록록리자전류.등삼、저삼태씨액관류;분별가입신복림、록리자전류조체제4,4'-이이류청기기-2,2'-이광산(DIDS)、α1수체조단제고서진,관찰전류변화.결과 저삼태씨액관류심방기세포,가기록도ICl.swell.용함유100μmol/L신복림적저삼태씨액관류,ICl.swell전류강도증가.재-90 mV,전류강도유(-1.11±0.55)pA/pF증가도(-1.56±0.69)pA/pF(P＜0.05,n=7);+40mV,유(3.24±2.04)pA/pF증가도(4.64±2.61)pA/pF(P＜0.01,n=7).저충효응위농도의뢰성,가입DIDS혹자용등삼관류액관류,해효응피역전.가입고서진1 μmol/L가이사신복림적량효관계곡선우이.결론 재인심방기세포신복림가이증강ICl.swell,저화재기타동물득도적결과불동.해현상시수차발현,표명신복림대ICl.swell적조절구유충속특이성.
Objective To study the function of phenylephrine, an α1-adrenoceptor agonists, in the regulation of swelling-activated chloride current ( ICl.swell) in human atrial myocytes by a whole-cell patch-clamp technique. Methods Atrial myocytes were isolated from specimens of right atrial appendage obtained from patients undergoing coronary artery bypass and enzymatically dissociated. The myocytes were perfused with isotonic bath solution (1.0T) or hyposmotic bath solution (0. 6-times isosmotic, 0. 6 T),and exposured to phenylephrine, 4,4'-diisothiocyanostilbene-2,2' disulfonicacid (DIDS), or prazosin, an α1-adrenoceptor antagonis respectively. The currents under different conditions were compared. Results ICl.swell evoked by hyposmotic bath solution was recorded. After approaching steady state values, subsequent exposure to 100 μmol/L phenylephrine caused enhancement of ICl.swell. The current was increased from (-1.11±0.55) pA/pF to ( - 1.56 ±0.69) pA/pF at -90 mV (P<0.05,n=7) and from (3.24±2.04) pA/pF to (4.64±2.61) pA/pF at +40 mV (P<0. 01,n=7) respectively. This effect was concentration-dependent, and could be reversed by DIDS or after exposure to the isotonic solution. Application of 1 μmol/L prazosin could attenuate the effect of phenylephrine. Conclusion Phenylephrine can enhance ICl.swell in human atrial myocytes, which is distinct from the reports in other species, indicating distinguished species-dependent variations in the modulation of ICl.swell, in atrial myocytes by phenylephrine.
